ArticleScientific reports2016
Prions efficiently cross the intestinal barrier after oral administration: Study of the bioavailability, and cellular and tissue distribution in vivo.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Evaluating the inter-species transmission risk of amyloid beta peptide aggregates via ingestion.Alzheimer's research & therapy · 2024Article
- The Current and Promising Oral Delivery Methods for Protein- and Peptide-Based Drugs.International journal of molecular sciences · 2024Review
- Preclinical Detection of Prions in Blood of Nonhuman Primates Infected with Variant Creutzfeldt-Jakob Disease.Emerging infectious diseases · 2020Article
- Oral and intravenous transmission of α-synuclein fibrils to mice.Acta neuropathologica · 2019Article
- Efficient prion disease transmission through common environmental materials.The Journal of biological chemistry · 2018Article
- How do PrPPathogens (Basel, Switzerland) · 2017Review
- Pathways of Prion Spread during Early Chronic Wasting Disease in Deer.Journal of virology · 2017Article
- PrPC expression and prion seeding activity in the alimentary tract and lymphoid tissue of deer.PloS one · 2017Article
- Increased Abundance of M Cells in the Gut Epithelium Dramatically Enhances Oral Prion Disease Susceptibility.PLoS pathogens · 2016Article
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Authors and funding
6 authors.
Funding
Abstract
Natural forms of prion diseases frequently originate by oral (p.o.) infection. However, quantitative information on the gastro-intestinal (GI) absorption of prions (i.e. the bioavailability and subsequent biodistribution) is mostly unknown. The main goal of this study was to evaluate the fate of prions after oral administration, using highly purified radiolabeled PrP(Sc). The results showed a bi-phasic reduction of PrP(Sc) with time in the GI, except for the ileum and colon which showed sustained increases peaking at 3-6 hr, respectively. Plasma and whole blood (125)I-PrP(Sc) reached maximal levels by 30 min and 3 hr, respectively, and blood levels were constantly higher than plasma. Upon crossing the GI-tract (125)I-PrP(Sc) became associated to blood cells, suggesting that binding to cells decreased the biological clearance of the agent. Size-exclusion chromatography revealed that oligomeric (125)I-PrP(Sc) were transported from the intestinal tract, and protein misfolding cyclic amplification showed that PrP(Sc) in organs and blood retained the typical prion self-replicating ability. Pharmacokinetic analysis found the oral bioavailability of (125)I-PrP(Sc) to be 33.6%. Interestingly, (125)I-PrP(Sc) reached the brain in a quantity equivalent to the minimum amount needed to initiate prion disease. Our findings provide a comprehensive and quantitative study of the fate of prions upon oral infection.
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